Urushiol-induced allergic contact dermatitis in the United States most commonly results from unexpected exposure to oils from plants in the sumac Family Anacardiaceae. Approximately 10 to 50 million Americans suffer from rashes resulting from exposure every year. In particular, the genus Toxicodendron species (which include Western and Eastern poison oak T. diversilobum, poison ivy T. radicans, and poison sumac or dogwood T. vernix) are distributed widely across North America. Other sources of urushiol include poison wood (in Florida and the Bahamas), and the sap (kiurushi) of the Asian lacquer tree (Toxicodendron vemiciflua) used as a varnish in Japanese lacquer ware, and cashew nut shells. (See, for example, Tucker and Swan (1998) NEJM, 339(4): 235.)
Reaction to urushiol is an immunological response to the bio-oxidized form of urushiol (the ortho-quinone). Approximately 50-70% of the U.S. population is either allergic to urushiol, or will become allergic to it upon sensitization by repeated exposure. Symptoms of allergic contact dermatitis from urushiol exposure (often referred to as Rhus dermatitis) vary from a mild annoyance to weeks of irritation and pain. Occasionally, exposure can lead to nephropathy and even to fatal systemic anaphylaxis. The monetary cost due to worker disability from urushiol-induced injuries is substantive: in the states of California, Washington and Oregon, it has been estimated that up to one third of forestry workers are temporarily disabled by poison oak dermatitis each year. In California, the medical costs associated with poison oak injuries accounts for up to 1% of the annual workers' compensation budget. It has been estimated that Toxicodendron dermatitis is responsible for 10% of the total U.S. Forest Services lost-time injuries. In 1988, NIOSH estimated that 1.07-1.65 million occupational skin injuries occurred yearly, with an estimated annual rate of 1.4 to 2.2 cases per 100 workers (8) the costs attributable to lost productivity, medical payments, and disability payments are very high. (See U.S. Centers for Disease Control; Leading work-related diseases and injuries—United States. MMWR, 1986 335:561-563).
Chemically, urushiol is a name given to a collection of related compounds that are 3-substituted catechols (1,2-benenediols), in which the long hydrophobic chain is a linear C15 or C17 alkyl chain containing 0-4 degrees of cis unsaturation (FIG. 1). The catechols with two, three, and four carbon-carbon double bonds (2-4 degrees of unsaturation) seem to be the most virulent in eliciting an allergic response. Each of the different members of the Toxicodendron species contain mixtures of the C15 or C17 alkyl chains, with various degrees of unsaturation.
They all share the catechol functionality in common, and a long, greasy alkyl chain that facilitates migration into the skin. In addition to direct contact with the toxic plants, exposure commonly occurs by transfer from animal fur, contaminated clothing, garden tools, fire-fighting equipment, forestry and sports equipment. There are a few commercially available products that can be applied prophylactically to protect the skin by creating a physical barrier using organoclays (for example, a lotion containing quaternium-18 bentonite is commercially available as IVYBLOCK from Enviroderm Pharmaceuticals, Inc.). However, the success of this strategy requires advanced planning By far the majority of allergic contact dermatitis cases from urushiol result from unexpected exposure.
A number of methods to treat poison ivy or poison oak have been investigated, including hyposensitization, but this process is involved and can have unfavorable side effects. Studies towards an immunological approach to desensitization have been pursued, but have not yet reached a level of practical application. The best treatment to date is to avoid contact with urushiol. As most patients are unaware that they have had contact with urushiol, a low cost, quick and inexpensive method of detection is warranted. There are many recommended methods to remove urushiol after recent contact, including water, soapy water, organic solvents, and a variety of commercially available solubilizing mixtures including TECHNU, IVYCLEANSE, ALL-STOP, ZANFEL (comprising fatty acid, alcohol, and the surfactant sodium lauroyl sarcosinate), and even DIAL ultra dishwashing soap. Thus the ability to detect urushiol before it transverses the skin will be extremely valuable in mitigating the suffering caused by contact with the various Toxicodendron species. In addition, continued re-exposure (chronic exposure) from repeated introduction of the oil to the patient (from door handles, shoelaces, etc.) is a considerable problem. As little as 0.001 mg of urushiol is enough to cause allergic contact dermatitis.
Treatment of the contact dermatitis usually involves a course of topical and/or enteric treatments with hydrocortisones, β-methasone, and other similar corticosteroids. Repeated exposure to either the original allergen or to a similar allergen can result in a severe hypersensitive immunoreaction, that is often extremely painful and, occasionally, fatal. There is therefore a particular need in the art for compounds and methods of treatment that can remove the allergen(s) prior to induction of an immune and/or allergic response, that can prevent the binding of the allergen(s) to an immunoglobulin or a cell-surface receptor, and/or that can be used to rapidly detect the presence of such allergen(s) so that other precautions may be used to remove the allergen(s) from the area of contact.
There is therefore a need in the art to provide for compositions and methods for detecting the presence of urushiol, inactivating urushiol, and removing urushiol from substrates (including, for example, skin and clothing).